Knockdown of alleviates ovalbumin-induced allergic rhinitis in mice by regulating NF-κB pathway.

Allergic rhinitis (AR), a type of chronic inflammatory disease that exists in the nasal mucosa, significantly impacts the quality of life. gene encodes an RNA helicase belonging to the DEAD-box protein family and is part of the DDX3 subfamily that affects the progression of multiple diseases. However, the specific role and mechanisms of in AR remain unclear. This study investigates the effects of knockdown on ovalbumin (OVA)-induced AR in mice. We found that is highly expressed in the nasal mucosa of AR mice. Knockdown of in OVA-induced AR mice significantly alleviated nasal manifestations, reduced immunoglobulin E and histamine levels, and improved nasal mucosal histopathology. Additionally, knockdown of suppressed secretion of inflammatory factor nuclear factor kappa B (NF-κB) phosphorylation, thereby mitigating local inflammatory responses. These findings suggested that targeting could offer a novel therapeutic strategy for managing AR by modulating the NF-κB pathway.